A 35-week gestation neonate weighing 1700 g is born to a mother who received no antenatal care. At 24 hours, the baby develops jitteriness, hypotonia, high-pitched cry, and seizures. Serum glucose is 68 mg/dL. Serum calcium is 5.8 mg/dL (ionized Ca 0.72 mmol/L). What is the pathophysiology of hypocalcemia in this preterm neonate?

• A Maternal hyperparathyroidism suppressing fetal PTH, leading to hypoparathyroidism neonatally
• B Abrupt discontinuation of placental calcium transfer combined with relative functional hypoparathyroidism and end-organ PTH resistance in prematurity ✓
• C DiGeorge syndrome with absent parathyroid glands
• D Hyperphosphatemia from cow's milk formula suppressing serum calcium

Explanation

Early neonatal hypocalcemia (within 72 hours) in preterm infants is caused by abrupt cessation of transplacental calcium transfer at birth, combined with functional hypoparathyroidism (the neonatal parathyroid gland is relatively unresponsive to hypocalcemia) and relative end-organ resistance to PTH. The preterm infant has immature calcium homeostasis. Calcitonin levels are also elevated in neonates, further reducing calcium. Treatment is with 10% calcium gluconate IV slowly (0.1–0.2 mL/kg over 10 minutes, with cardiac monitoring). Late neonatal hypocalcemia (>1 week) is more likely due to high phosphate load from cow's milk.

Reference: Ghai Essential Pediatrics, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.